Renal Physiology

Renal physiology underpins much of urologic practice, from interpreting electrolyte and acid-base disturbances to recognizing and managing acute kidney injury. This topic reviews nephron segment function, the handling of sodium, potassium, and acid-base balance, and the causes and management of kidney injury and renal tubular acidoses.

Normal Renal Function and Balances

Nephron Basics

• Proximal convoluted tubule: reabsorbs 65% Na, K, Ca, 80% Phos, H2O, bicarb, and 100% glucose and amino acids, also generates ammonia from glutamine (urinary acidification)
• Loop of Henle: absorbs 25-30% Na and concentrates the interstitium, descending limb water permeable, ascending limb water impermeable
• Distal convoluted tubule: absorbs Na, Ca
• Collecting tubule: absorb Na via principal cells, H via intercalated cells, K by both

Sodium Balance

• Regulated by ADH (free water)
• Assess fluid status: skin turgor, blood pressure
• Sodium repletion: 3% saline at 1mL/kg/hr, do not exceed 8-12mmol/L/d (can cause cerebral demyelination)

Potassium Balance

• Hypokalemia: seen with GI loss, renal loss, systemic alkalosis, medications, postobstructive diuresis, and hyperaldosteronism
• Hyperkalemia: seen with impaired renal excretion, systemic acidosis
• Bicarbonate, insulin + glucose, and albuterol used to drive K intracellularly, does not cause K losses
• K excretion: induce with kayexalate or lokelma (K-binding exchange resin), diuretics, and hemodialysis
• Calcium gluconate: prevents cardiac complications (stabilizes myocytes) when EKG changes seen

Acid/Base Balance

• Concentration alkalosis: volume depletion causes Na retention, bicarb absorption, and net loss of H
• Respiratory acidosis: elevated CO2 leads to increased renal H secretion
• Renal failure: decreased bicarb filtration leads to increased H loss
• Hyperaldosteronism: increased Na absorption causes increased H losses

Kidney Injury

Acute Kidney Injury Causes

• Prerenal AKI: caused by renal hypoperfusion, decreased FENa, reversible after removing underlying cause and improving renal perfusion
• Intrarenal AKI: caused by glomerular/tubular injury, requires diagnosis and treatment of specific cause
• Postrenal AKI: caused by urinary tract obstruction, can result in postobstructive diuresis after resolution with resultant water/salt wasting
• Acute interstitial nephritis (AIN): rash 15%, fever 27%, eosinophilia 23%, diagnose with high suspicion, WBC casts, and renal biopsy
• Renal vein thrombosis: seen with nephrotic syndrome and malignancy, presents with flank pain + hematuria + elevated LDH + swollen kidney on imaging
• Assessing AKI: volume status, cardiac history, liver/renal failure, DM, recent surgery, medications, contrast, bleeding, serum/urine electrolytes
• Fractional Excretion of Na (FENa): (UNa * SCr) / (SNa * UCr), cutoff 1%
• Fractional Excretion of Urea (FEUrea): (Urea * SCr) / (SBUN * UCr), cutoff 35%

Management of Intrarenal AKI

• Contrast nephropathy: unclear if a true diagnosis, prevent with IV hydration
• Rhabdomyolysis: IV hydration + bicarbonate (monitor in ICU)
• Tumor: caused by uric acid crystal precipitation and hyperphosphatemia, can consider prophylactic rasburicase (converts uric acid to allantoin)
• Can give loop diuretics, good response indicates favorable prognosis, diuretic use does not worsen or improve AKI recovery

Renal Tubule Acidoses

• Type I: unable to secrete H in distal nephron, causes hyperchloremic metabolic acidosis, urine pH > 5.5, low serum bicarb, low urine citrate, CaPhos stones
• Type II: unable to absorb bicarb in proximal tubule
• Type IV: decreased H and K secretion in collecting duct